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10.4161/19490976.2014.969989 http://scihub22266oqcxt.onion/10.4161/19490976.2014.969989 C4615906!4615906!25483338     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25483338&cmd=llinks): Failed to open stream: HTTP request failed! 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The bacterial genotoxin colibactin promotes colon tumor growth by modifying the tumor microenvironment |pdf=|usr=}}{{25483338}} gab.com Text The bacterial genotoxin colibactin promotes colon tumor growth by modifying the tumor microenvironment JO: Gut Microbes http://www.kidney.de/pget.php?&tw=1&pmid=25483338 #FOAvip The gut microbiota is suspected to promote colorectal cancer (CRC). Escherichia coli are more frequently found in CCR biopsies than in healthy mucosa; furthermore, the majority of mucosa-associated E. coli isolated from CCR harbors the pks genomic island (pks+ E. coli) that is responsible for the synthesis of colibactin, a genotoxic compound. We have recently reported that transient contact of a few malignant cells with colibactin-producing E. coli increases tumor growth in a xenograft mouse model. Growth is sustained by cellular senescence that is accompanied by the production of growth factors. We demonstrated that cellular senescence is a consequence of the pks+ E. coli-induced alteration of p53 SUMOylation, an essential post-translational modification in eukaryotic cells. The underlying mechanisms for this process involve the induction of miR-20a-5p expression, which targets SENP1, a key protein in the regulation of the SUMOylation process. These results are consistent with the expression of SENP1, miR-20a-5p and growth factors that are observed in a CRC mouse model and in human CCR biopsies colonized by pks+ E. coli. Overall, the data reveal a new paradigm for carcinogenesis in which pks+ E. coli infection induces cellular senescence characterized by the production of growth factors that promote the proliferation of uninfected cells and, subsequently, tumor growth. Twit Text FOAVip The bacterial genotoxin colibactin promotes colon tumor growth by modifying the tumor microenvironment ????Gut Microbes http://www.kidney.de/pget.php?&tw=1&pmid=25483338 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25483338 #FOAvip English Wikipedia <ref>{{Cite pmid|25483338}}</ref> The bacterial genotoxin colibactin promotes colon tumor growth by modifying the tumor microenvironment #MMPMID25483338 Dalmasso G; Cougnoux A; Delmas J; Darfeuille-Michaud A; Bonnet R Gut Microbes 2014[]; 5 (5): 675-80 PMID25483338show ga The gut microbiota is suspected to promote colorectal cancer (CRC). Escherichia coli are more frequently found in CCR biopsies than in healthy mucosa; furthermore, the majority of mucosa-associated E. coli isolated from CCR harbors the pks genomic island (pks+ E. coli) that is responsible for the synthesis of colibactin, a genotoxic compound. We have recently reported that transient contact of a few malignant cells with colibactin-producing E. coli increases tumor growth in a xenograft mouse model. Growth is sustained by cellular senescence that is accompanied by the production of growth factors. We demonstrated that cellular senescence is a consequence of the pks+ E. coli-induced alteration of p53 SUMOylation, an essential post-translational modification in eukaryotic cells. The underlying mechanisms for this process involve the induction of miR-20a-5p expression, which targets SENP1, a key protein in the regulation of the SUMOylation process. These results are consistent with the expression of SENP1, miR-20a-5p and growth factors that are observed in a CRC mouse model and in human CCR biopsies colonized by pks+ E. coli. Overall, the data reveal a new paradigm for carcinogenesis in which pks+ E. coli infection induces cellular senescence characterized by the production of growth factors that promote the proliferation of uninfected cells and, subsequently, tumor growth. äThe bacterial genotoxin colibactin promotes colon tumor growth by modi(epmc).pdf DeepDyve Pubget Overpricing